Study detects immune changes up to 10 years before IBD is diagnosed

Researchers at the Icahn School of Medicine at Mount Sinai have identified immune system changes that can be detected up to 10 years before inflammatory bowel disease (IBD) develops, offering new insight into how the disease begins.

Published July 21 in Gut, the study is one of the most comprehensive investigations to date of the preclinical phase of IBD. Using antibody profiling technology, researchers analyzed nearly 2,000 blood samples collected over about a decade from people who later developed Crohn’s disease or ulcerative colitis. They identified unique antibody signatures against viruses and bacteria—particularly Epstein-Barr virus and bacterial flagellins—that were present years before diagnosis, suggesting that abnormal immune activity begins long before the disease becomes clinically apparent.

“IBD does not develop overnight,” said Saurabh Mehandru, MD, corresponding author of the study and Professor of Medicine (Gastroenterology) at the Icahn School of Medicine at Mount Sinai. “Our findings show that the immune system is already changing years before patients experience their first symptoms. By understanding these early immune changes, we hope to uncover the biological events that trigger disease and ultimately develop strategies to identify, and one day prevent, IBD before it starts.”

Researchers profiled antibody responses against 357,000 viral, bacterial, and other antigens in blood samples collected approximately 10 years, 4 years, and 2 years before diagnosis, as well as shortly after diagnosis. The study included 200 people who later developed Crohn’s disease, 200 people who developed ulcerative colitis, and 100 healthy individuals. Antibody responses evolved over time and differed significantly between people who developed IBD and those who remained healthy. Many of the strongest signals were already detectable at the earliest time point, approximately 10 years before diagnosis.

Among the most striking findings were elevated antibody responses against Epstein-Barr virus and bacterial flagellins in people who later developed Crohn’s disease. These immune signatures remained detectable years before diagnosis and support growing evidence that interactions between infections, the gut microbiome, and the immune system may contribute to the earliest stages of IBD. The findings also support the theory of molecular mimicry, in which immune responses to viruses or bacteria may inadvertently target the body’s own tissues.

While additional research is needed before these antibody signatures can be used clinically, the findings could eventually help identify people at increased risk for IBD, particularly relatives of patients with the disease, and guide future prevention strategies.

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